The long term objective of this project is to develop models of motor control that can be used to understand the defective motor control mechanisms of Parkinson's disease, Huntington's disease and the movement deficits that arise from cerebellar lesions. The proposal has five primary aims. The first is to determine the extent to which patterns of muscle activation observed at the elbow occur at joints such as the wrist and thumb. The aim is to reconcile two sets of conflicting results. The second is to determine the extent to which the findings of single joint movements can be extrapolated to multijoint movements in patients with Parkinson's disease and aged matched controls. The third aim is to investigate how movement speed and movement distance is controlled at different joints in patients with Parkinson's disease and Huntington's disease. The experiments will focus on whether the motor deficits associated with Parkinson's disease can best be characterized in terms of a rate limitation in the ability to generate force or whether many individuals with Parkinson's disease have tremor (even if clinically non-detectable) and that movement control is impaired by the presence of rhythmically activated motoneuron pools that limit the ability to prolong the duration of excitation to motoneuron pools. The fourth aim is to determine the extent to which the movement deficits of Parkinson's disease are predominantly distal. That is, movements made by the wrist win show greater deficits than movements made by the elbow or shoulder. The fifth aim is to confirm that patients with lateral cerebellar lesions have specific deficits in timing the activation of the antagonist muscle that are not present in age matched controls or in patients with medial cerebellar lesions. The results of these experiments will demonstrate the extent to which the findings of the dual strategy hypothesis of motor control can be extended beyond rapid, single degree of freedom elbow movements to encompass a much broader range of tasks performed by patients with basal ganglia and cerebellar movement deficits. Further insights into how the motor neuron pools of patients are controlled will be a useful step inward from kinematic observations. This may further our understanding of the more fundamental but less accessible central deficits that play the ultimate causal roles in the disease processes. The experimental data might ultimately be useful in developing models of motor control that will aid in detecting and evaluating disorders of movement as well as serving as a useful testing protocol for various therapeutic interventions.